Rice (Oryza sativa) is the staple food crop for more than 50% of the world's popula-tion and rice blast disease is a major factor influencing stable rice production. A thorough understanding of rice host defense mechanisms is essential for breeding rice varieties conferring durable resistance to rice blast. Recently, the Research Group of Plant Disease Resistance and Functional Genomics have published two re-search papers on PLOS Pathogens and Cell Host & Microbe about the Magnaporthe oryzae pathogenesis mechanism and rice resistance mechanism. The research work presented in these papers was selected as one of the Top 10 Science & Technology Advances of CAAS in 2018.

For M. oryzae pathogenesis mechanism, they found that M. oryzae effector AvrPiz-t interacts with the rice plasma-membrane-localized K+ channel protein OsAKT1 and specifically suppresses the OsAKT1-mediated K+ currents. Genetic and phenotypic analyses show that loss of OsAKT1 leads to decreased K+ content and reduced resistance against M. oryzae. Strikingly, AvrPiz-t interferes with the association of OsAKT1 with its upstream regulator, the cytoplasmic kinase OsCIPK23, which also plays a positive role in K+ absorption and resistance to M. oryzae. Furthermore, the authors show a direct correlation between blast disease resistance and external K+ status in rice plants. Together, these results present a novel mechanism by which a pathogen suppresses plant host immunity by modulating a host K+ channel.

For rice resistance mechanism, they reported map-based cloning and characteriza-tion of SDS2 that encodes an S-domain RLK. Mutation of SDS2 leads to reduced resistance to the blast fungus M. oryzae. Conversely, SDS2 over-expression enhances resistance to M. oryzae and induces defense gene expression. They also find that SDS2 interacts with and phosphorylates SPL11, which in turn ubiquitinates SDS2. SDS2 positively regulates rice immunity and interacts with RLCKs OsRLCK118 and OsRLCK176, which are also positive regulators of rice immunity. Furthermore, OsRLCK118 interacts with and phosphorylates the NADPH oxidase OsRbohB to induce ROS burst during pathogen infection. Taken together, they show that SDS2 is a monocot-specific RLK that plays a positive role in the regulation of PCD and immunity by complexing with the E3 ligase SPL11 and OsRLCK118/176 in rice.